Goiter pathophysiology: Difference between revisions

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{{CMG}}; {{AE}} {{ARK}}
{{CMG}}; {{AE}} {{ARK}}
==Overview==
==Overview==
When the [[TRH]]-[[TSH]] thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland. Increased [[TSH]] production is trigerred by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in [[TSH]] leads to increased cellularity and [[hyperplasia]] of the thyroid gland and when this process is continuous, it leads to goiter.
When the [[TRH]]-[[TSH]] [[thyroid hormone]] [[axis]] is interfered, it results in the structural and functional changes of the [[thyroid gland]]. Increased [[TSH]] production is trigerred by a [[deficiency]] in [[thyroid hormone]] [[synthesis]] or intake. In order to normalize [[thyroid hormone]] levels, the increase in [[TSH]] leads to increased cellularity and [[hyperplasia]] of the [[thyroid gland]] and when this process is continuous, it leads to goiter.


==Pathophysiology==
==Pathophysiology==


'''Pathogenesis:'''<ref name="Rapoport1991">{{cite journal|last1=Rapoport|first1=Basil|title=Pathophysiology of Hashimoto's Thyroiditis and Hypothyroidism|journal=Annual Review of Medicine|volume=42|issue=1|year=1991|pages=91–96|issn=0066-4219|doi=10.1146/annurev.me.42.020191.000515}}</ref><ref name="Larsen1972">{{cite journal|last1=Larsen|first1=P.R.|title=Triiodothyronine: Review of recent studies of its physiology and pathophysiology in man|journal=Metabolism|volume=21|issue=11|year=1972|pages=1073–1092|issn=00260495|doi=10.1016/0026-0495(72)90038-8}}</ref><ref name="GaitanWahner1969">{{cite journal|last1=Gaitan|first1=Eduardo|last2=Wahner|first2=Heinz W.|last3=Cuello|first3=Carlos|last4=Correa|first4=Pelayo|last5=Jubiz|first5=William|last6=Gaitan|first6=Jorge E.|title=Endemic Goiter in the Cauca Valley: II. Studies of Thyroid Pathophysiology1|journal=The Journal of Clinical Endocrinology & Metabolism|volume=29|issue=5|year=1969|pages=675–683|issn=0021-972X|doi=10.1210/jcem-29-5-675}}</ref><ref name="pmid2114018">{{cite journal |vauthors=Elte JW, Bussemaker JK, Haak A |title=The natural history of euthyroid multinodular goitre |journal=Postgrad Med J |volume=66 |issue=773 |pages=186–90 |year=1990 |pmid=2114018 |pmc=2429462 |doi= |url=}}</ref><ref name="pmid2239979">{{cite journal |vauthors=Berghout A, Wiersinga WM, Smits NJ, Touber JL |title=Interrelationships between age, thyroid volume, thyroid nodularity, and thyroid function in patients with sporadic nontoxic goiter |journal=Am. J. Med. |volume=89 |issue=5 |pages=602–8 |year=1990 |pmid=2239979 |doi= |url=}}</ref><ref name="SotoImas1967">{{cite journal|last1=Soto|first1=Roberto J.|last2=Imas|first2=Berta|last3=Brunengo|first3=Ana M.|last4=Goldberg|first4=David|last5=Burian|first5=Rosa|last6=Gnocchi|first6=Luisa|title=Endemic Goiter in Misiones, Argentina: Pathophysiology Related to Immunological Phenomena|journal=The Journal of Clinical Endocrinology & Metabolism|volume=27|issue=11|year=1967|pages=1581–1587|issn=0021-972X|doi=10.1210/jcem-27-11-1581}}</ref><ref name="pmid9677510">{{cite journal |vauthors=Gärtner R, Dugrillon A |title=[From iodine deficiency to goiter. Pathophysiology of iron deficiency goiter] |language=German |journal=Internist (Berl) |volume=39 |issue=6 |pages=566–73 |year=1998 |pmid=9677510 |doi= |url=}}</ref><ref name="Peteiro-GonzalezLee2010">{{cite journal|last1=Peteiro-Gonzalez|first1=D.|last2=Lee|first2=J.|last3=Rodriguez-Fontan|first3=J.|last4=Castro-Piedras|first4=I.|last5=Cameselle-Teijeiro|first5=J.|last6=Beiras|first6=A.|last7=Bravo|first7=S. B.|last8=Alvarez|first8=C. V.|last9=Hardy|first9=D. M.|last10=Targovnik|first10=H. M.|last11=Arvan|first11=P.|last12=Lado-Abeal|first12=J.|title=New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter|journal=The Journal of Clinical Endocrinology & Metabolism|volume=95|issue=7|year=2010|pages=3522–3526|issn=0021-972X|doi=10.1210/jc.2009-2109}}</ref><ref name="Capen1992">{{cite journal|last1=Capen|first1=C.C.|title=Pathophysiology of chemical injury of the thyroid gland|journal=Toxicology Letters|volume=64-65|year=1992|pages=381–388|issn=03784274|doi=10.1016/0378-4274(92)90211-2}}</ref><ref name="MaceriSullivan1986">{{cite journal|last1=Maceri|first1=Dennis R.|last2=Sullivan|first2=Michael J.|last3=McClatchney|first3=Kenneth D.|title=AUTOIMMUNE THYROIDITIS|journal=The Laryngoscope|volume=96|issue=1|year=1986|pages=82???86|issn=0023-852X|doi=10.1288/00005537-198601000-00015}}</ref><ref name="NeumannWillgerodt1999">{{cite journal|last1=Neumann|first1=Susanne|last2=Willgerodt|first2=Helmut|last3=Ackermann|first3=Frank|last4=Reske|first4=Andreas|last5=Jung|first5=Martin|last6=Reis|first6=André|last7=Paschke|first7=Ralf|title=Linkage of Familial Euthyroid Goiter to the Multinodular Goiter-1 Locus and Exclusion of the Candidate Genes Thyroglobulin, Thyroperoxidase, and Na+/I−Symporter1|journal=The Journal of Clinical Endocrinology & Metabolism|volume=84|issue=10|year=1999|pages=3750–3756|issn=0021-972X|doi=10.1210/jcem.84.10.6023}}</ref>  
'''Pathogenesis:'''<ref name="Rapoport1991">{{cite journal|last1=Rapoport|first1=Basil|title=Pathophysiology of Hashimoto's Thyroiditis and Hypothyroidism|journal=Annual Review of Medicine|volume=42|issue=1|year=1991|pages=91–96|issn=0066-4219|doi=10.1146/annurev.me.42.020191.000515}}</ref><ref name="Larsen1972">{{cite journal|last1=Larsen|first1=P.R.|title=Triiodothyronine: Review of recent studies of its physiology and pathophysiology in man|journal=Metabolism|volume=21|issue=11|year=1972|pages=1073–1092|issn=00260495|doi=10.1016/0026-0495(72)90038-8}}</ref><ref name="GaitanWahner1969">{{cite journal|last1=Gaitan|first1=Eduardo|last2=Wahner|first2=Heinz W.|last3=Cuello|first3=Carlos|last4=Correa|first4=Pelayo|last5=Jubiz|first5=William|last6=Gaitan|first6=Jorge E.|title=Endemic Goiter in the Cauca Valley: II. Studies of Thyroid Pathophysiology1|journal=The Journal of Clinical Endocrinology & Metabolism|volume=29|issue=5|year=1969|pages=675–683|issn=0021-972X|doi=10.1210/jcem-29-5-675}}</ref><ref name="pmid2114018">{{cite journal |vauthors=Elte JW, Bussemaker JK, Haak A |title=The natural history of euthyroid multinodular goitre |journal=Postgrad Med J |volume=66 |issue=773 |pages=186–90 |year=1990 |pmid=2114018 |pmc=2429462 |doi= |url=}}</ref><ref name="pmid2239979">{{cite journal |vauthors=Berghout A, Wiersinga WM, Smits NJ, Touber JL |title=Interrelationships between age, thyroid volume, thyroid nodularity, and thyroid function in patients with sporadic nontoxic goiter |journal=Am. J. Med. |volume=89 |issue=5 |pages=602–8 |year=1990 |pmid=2239979 |doi= |url=}}</ref><ref name="SotoImas1967">{{cite journal|last1=Soto|first1=Roberto J.|last2=Imas|first2=Berta|last3=Brunengo|first3=Ana M.|last4=Goldberg|first4=David|last5=Burian|first5=Rosa|last6=Gnocchi|first6=Luisa|title=Endemic Goiter in Misiones, Argentina: Pathophysiology Related to Immunological Phenomena|journal=The Journal of Clinical Endocrinology & Metabolism|volume=27|issue=11|year=1967|pages=1581–1587|issn=0021-972X|doi=10.1210/jcem-27-11-1581}}</ref><ref name="pmid9677510">{{cite journal |vauthors=Gärtner R, Dugrillon A |title=[From iodine deficiency to goiter. Pathophysiology of iron deficiency goiter] |language=German |journal=Internist (Berl) |volume=39 |issue=6 |pages=566–73 |year=1998 |pmid=9677510 |doi= |url=}}</ref><ref name="Peteiro-GonzalezLee2010">{{cite journal|last1=Peteiro-Gonzalez|first1=D.|last2=Lee|first2=J.|last3=Rodriguez-Fontan|first3=J.|last4=Castro-Piedras|first4=I.|last5=Cameselle-Teijeiro|first5=J.|last6=Beiras|first6=A.|last7=Bravo|first7=S. B.|last8=Alvarez|first8=C. V.|last9=Hardy|first9=D. M.|last10=Targovnik|first10=H. M.|last11=Arvan|first11=P.|last12=Lado-Abeal|first12=J.|title=New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter|journal=The Journal of Clinical Endocrinology & Metabolism|volume=95|issue=7|year=2010|pages=3522–3526|issn=0021-972X|doi=10.1210/jc.2009-2109}}</ref><ref name="Capen1992">{{cite journal|last1=Capen|first1=C.C.|title=Pathophysiology of chemical injury of the thyroid gland|journal=Toxicology Letters|volume=64-65|year=1992|pages=381–388|issn=03784274|doi=10.1016/0378-4274(92)90211-2}}</ref><ref name="MaceriSullivan1986">{{cite journal|last1=Maceri|first1=Dennis R.|last2=Sullivan|first2=Michael J.|last3=McClatchney|first3=Kenneth D.|title=AUTOIMMUNE THYROIDITIS|journal=The Laryngoscope|volume=96|issue=1|year=1986|pages=82???86|issn=0023-852X|doi=10.1288/00005537-198601000-00015}}</ref><ref name="NeumannWillgerodt1999">{{cite journal|last1=Neumann|first1=Susanne|last2=Willgerodt|first2=Helmut|last3=Ackermann|first3=Frank|last4=Reske|first4=Andreas|last5=Jung|first5=Martin|last6=Reis|first6=André|last7=Paschke|first7=Ralf|title=Linkage of Familial Euthyroid Goiter to the Multinodular Goiter-1 Locus and Exclusion of the Candidate Genes Thyroglobulin, Thyroperoxidase, and Na+/I−Symporter1|journal=The Journal of Clinical Endocrinology & Metabolism|volume=84|issue=10|year=1999|pages=3750–3756|issn=0021-972X|doi=10.1210/jcem.84.10.6023}}</ref>  
*Goiters may occur as a result of either [[hypothyroidism]], [[hyperthyroidism]], or when the levels of thyroid hormone are normal.
*Goiters may occur as a result of either [[hypothyroidism]], [[hyperthyroidism]], or even with normal levels of [[thyroid hormone]].
*Thyroid enlargement (goiter) and [[hypothyroidism]] may occur due to compensatory responses as a result of a severe underlying disorder.
*[[Thyroid enlargement]] (goiter) and [[hypothyroidism]] may occur due to compensatory responses as a result of a severe underlying [[disorder]].
*When the thyroid gland can't secrete enough thyroid hormone to cater to the [[metabolic]] requirements, it may lead to simple goiter.
*When the [[thyroid gland]] cannot secrete enough [[thyroid hormone]] to cater to the [[metabolic]] requirements, it may lead to simple goiter.
*In order to compensate for inadequate hormone synthesis the thyroid gland enlarges, this type of compensation overcomes mild to moderate hormonal impairment.
*In order to compensate for inadequate [[hormone]] synthesis the [[thyroid gland]] enlarges, this type of compensation overcomes mild to moderate [[hormonal]] impairment.
*When the [[TRH]]-[[TSH]] thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland.
*When the [[TRH]]-[[TSH]] [[thyroid hormone]] [[axis]] is interfered, it results in the structural and functional changes of the [[thyroid gland]].
*Increased [[TSH]] production is trigerred by a deficiency in thyroid hormone synthesis or intake.
*Increased [[TSH]] production is triggered by a [[deficiency]] in [[thyroid hormone]] [[synthesis]] or intake.
*In order to normalize thyroid hormone levels, the increase in [[TSH]] leads to increased cellularity and [[hyperplasia]] of the thyroid gland and when this process is continuous, it leads to goiter.
*In order to normalize [[thyroid hormone]] levels, the increase in [[TSH]] leads to increased cellularity and [[hyperplasia]] of the [[thyroid gland]] and when this [[Process (anatomy)|process]] is continuous, it leads to goiter.
*Thyroid hormone deficiency may be related to [[iodine deficiency]], inborn errors of thyroid hormone synthesis and goitrogens.
*[[Thyroid hormone]] [[deficiency]] may be related to [[iodine deficiency]], inborn errors of [[thyroid hormone]] [[synthesis]] and goitrogens.
*Goiters may from as a result of a many [[TSH]] receptor agonists. The [[TSH]] receptor gets stimulated under the following conditions:
*Goiters may from as a result of a many [[TSH]] receptor agonists. The [[TSH]] receptor gets stimulated under the following conditions:
**Adenoma of the [[pituitary]]
**[[Adenoma]] of the [[pituitary]]
**Adenoma of the [[hypothalamus]]  
**[[Adenoma]] of the [[hypothalamus]]  
**Pituitary resistance to thyroid hormone
**Pituitary resistance to [[thyroid hormone]]
**[[TSH]] receptor antibodies
**[[TSH]] receptor [[antibodies]]
**Tumors producing [[hCG]] (human chorionic gonadotropin)
**[[Tumors]] producing [[hCG]] (human chorionic gonadotropin)


*'''<u>The pathophysiological consequences of goitres results from one of the following</u>:'''
*'''<u>The pathophysiological consequences of goitres results from one of the following</u>:'''
**''The effect of thyroid hormone dysfunction''
**''The effect of [[thyroid hormone]] dysfunction''
**''The effect of enlarged thyroid gland''
**''The effect of [[enlarged thyroid gland]]''
**''The effect of primary disease causing goitre''
**''The effect of primary disease causing goitre''


*'''''The effect of thyroid hormone dysfunction:'''''
*'''''The effect of thyroid hormone dysfunction:'''''
**Thyroid hyperfunction (hyperthyroidism) → Features of hyperthyroidism
**Thyroid [[hyperfunction]] ([[hyperthyroidism]]) → Features of [[hyperthyroidism]]
**Thyroid hypofunction (hypothyroidism) → Features of hypothyroidism
**[[Hypofunctioning thyroid|Thyroid hypofunction]] ([[hypothyroidism]]) → Features of [[hypothyroidism]]


*'''''The effect of enlarged thyroid gland:'''''
*'''''The effect of enlarged thyroid gland:'''''
**Effect on the [[trachea]] results in [[dyspnea]]
**Effect on the [[trachea]] results in [[dyspnea]]
**Effect on the [[esophagus]] results in [[dysphagia]]
**Effect on the [[esophagus]] results in [[dysphagia]]
**Effect on the [[superior venacava]] results in distended neck veins
**Effect on the [[superior vena cava]] results in distended [[neck veins]]
**Effect on the [[recurrent laryngeal nerve]] results in [[hoarseness]] of voice
**Effect on the [[recurrent laryngeal nerve]] results in [[hoarseness]] of voice


*'''''The effect of primary disease causing goitre:'''''
*'''''The effect of primary disease causing goitre:'''''
**The effect depends on the underlying disease
**The effect depends on the underlying [[disease]]


==Genetics==
==Genetics==
*Goiter may be caused by a [[mutation]] in the following genes which vary from one family to the other: <ref name="pmid10821321">{{cite journal |vauthors=Brix TH, Hegedüs L |title=Genetic and environmental factors in the aetiology of simple goitre |journal=Ann. Med. |volume=32 |issue=3 |pages=153–6 |year=2000 |pmid=10821321 |doi= |url=}}</ref> <ref name="pmid12588808">{{cite journal |vauthors=Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N |title=The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance |journal=Endocr. Rev. |volume=24 |issue=1 |pages=48–77 |year=2003 |pmid=12588808 |doi=10.1210/er.2001-0029 |url=}}</ref> <ref name="TargovnikEsperante2010">{{cite journal|last1=Targovnik|first1=Héctor M.|last2=Esperante|first2=Sebastián A.|last3=Rivolta|first3=Carina M.|title=Genetics and phenomics of hypothyroidism and goiter due to thyroglobulin mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=44–55|issn=03037207|doi=10.1016/j.mce.2010.01.009}}</ref> <ref name="SpitzwegMorris2010">{{cite journal|last1=Spitzweg|first1=Christine|last2=Morris|first2=John C.|title=Genetics and phenomics of hypothyroidism and goiter due to NIS mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=56–63|issn=03037207|doi=10.1016/j.mce.2010.02.007}}</ref> <ref name="MorenoVisser2010">{{cite journal|last1=Moreno|first1=José C.|last2=Visser|first2=Theo J.|title=Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=91–98|issn=03037207|doi=10.1016/j.mce.2010.03.010}}</ref> <ref name="pmid4980080">{{cite journal |vauthors=Fraser GR |title=The genetics of thyroid disease |journal=Prog Med Genet |volume=6 |issue= |pages=89–115 |year=1969 |pmid=4980080 |doi= |url=}}</ref>
*Goiter may be caused by a [[mutation]] in the following [[genes]] which vary from one [[family]] to the other: <ref name="pmid10821321">{{cite journal |vauthors=Brix TH, Hegedüs L |title=Genetic and environmental factors in the aetiology of simple goitre |journal=Ann. Med. |volume=32 |issue=3 |pages=153–6 |year=2000 |pmid=10821321 |doi= |url=}}</ref> <ref name="pmid12588808">{{cite journal |vauthors=Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N |title=The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance |journal=Endocr. Rev. |volume=24 |issue=1 |pages=48–77 |year=2003 |pmid=12588808 |doi=10.1210/er.2001-0029 |url=}}</ref> <ref name="TargovnikEsperante2010">{{cite journal|last1=Targovnik|first1=Héctor M.|last2=Esperante|first2=Sebastián A.|last3=Rivolta|first3=Carina M.|title=Genetics and phenomics of hypothyroidism and goiter due to thyroglobulin mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=44–55|issn=03037207|doi=10.1016/j.mce.2010.01.009}}</ref> <ref name="SpitzwegMorris2010">{{cite journal|last1=Spitzweg|first1=Christine|last2=Morris|first2=John C.|title=Genetics and phenomics of hypothyroidism and goiter due to NIS mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=56–63|issn=03037207|doi=10.1016/j.mce.2010.02.007}}</ref> <ref name="MorenoVisser2010">{{cite journal|last1=Moreno|first1=José C.|last2=Visser|first2=Theo J.|title=Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=91–98|issn=03037207|doi=10.1016/j.mce.2010.03.010}}</ref> <ref name="pmid4980080">{{cite journal |vauthors=Fraser GR |title=The genetics of thyroid disease |journal=Prog Med Genet |volume=6 |issue= |pages=89–115 |year=1969 |pmid=4980080 |doi= |url=}}</ref>
:*[[Thyroglobulin]] (Tg) gene
:*[[Thyroglobulin]] (Tg) gene
:*[[Thyroid-stimulating hormone receptor]] ([[TSHR]]) gene
:*Thyroid-stimulating hormone receptor (TSHR) gene
:*Na+/I- symporter (NIS) gene <ref name="pmid24311738">{{cite journal| author=Portulano C, Paroder-Belenitsky M, Carrasco N| title=The Na+/I- symporter (NIS): mechanism and medical impact. | journal=Endocr Rev | year= 2014 | volume= 35 | issue= 1 | pages= 106-49 | pmid=24311738 | doi=10.1210/er.2012-1036 | pmc=3895864 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24311738  }} </ref>
:*Na+/I- symporter (NIS) gene <ref name="pmid24311738">{{cite journal| author=Portulano C, Paroder-Belenitsky M, Carrasco N| title=The Na+/I- symporter (NIS): mechanism and medical impact. | journal=Endocr Rev | year= 2014 | volume= 35 | issue= 1 | pages= 106-49 | pmid=24311738 | doi=10.1210/er.2012-1036 | pmc=3895864 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24311738  }} </ref>


Line 54: Line 54:


==Gross Pathology==
==Gross Pathology==
*On gross pathology the following features are observed: <ref name="pmid13263417">{{cite journal| author=MORTENSEN JD, WOOLNER LB, BENNETT WA| title=Gross and microscopic findings in clinically normal thyroid glands. | journal=J Clin Endocrinol Metab | year= 1955 | volume= 15 | issue= 10 | pages= 1270-80 | pmid=13263417 | doi=10.1210/jcem-15-10-1270 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13263417  }} </ref> <ref name="pmid25996397">{{cite journal| author=| title=Reorganized text. | journal=JAMA Otolaryngol Head Neck Surg | year= 2015 | volume= 141 | issue= 5 | pages= 428 | pmid=25996397 | doi=10.1001/jamaoto.2015.0540 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25996397  }} </ref> <ref name="pmid12588812">{{cite journal| author=Hegedüs L, Bonnema SJ, Bennedbaek FN| title=Management of simple nodular goiter: current status and future perspectives. | journal=Endocr Rev | year= 2003 | volume= 24 | issue= 1 | pages= 102-32 | pmid=12588812 | doi=10.1210/er.2002-0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12588812  }} </ref>
*On [[gross pathology]] the following features are observed: <ref name="pmid13263417">{{cite journal| author=MORTENSEN JD, WOOLNER LB, BENNETT WA| title=Gross and microscopic findings in clinically normal thyroid glands. | journal=J Clin Endocrinol Metab | year= 1955 | volume= 15 | issue= 10 | pages= 1270-80 | pmid=13263417 | doi=10.1210/jcem-15-10-1270 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13263417  }} </ref> <ref name="pmid25996397">{{cite journal| author=| title=Reorganized text. | journal=JAMA Otolaryngol Head Neck Surg | year= 2015 | volume= 141 | issue= 5 | pages= 428 | pmid=25996397 | doi=10.1001/jamaoto.2015.0540 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25996397  }} </ref> <ref name="pmid12588812">{{cite journal| author=Hegedüs L, Bonnema SJ, Bennedbaek FN| title=Management of simple nodular goiter: current status and future perspectives. | journal=Endocr Rev | year= 2003 | volume= 24 | issue= 1 | pages= 102-32 | pmid=12588812 | doi=10.1210/er.2002-0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12588812  }} </ref>
**Enlarged thyroid gland
**[[Enlarged thyroid gland]]
**Multiple nodules lacking fibrous capsule
**Multiple nodules lacking [[fibrous capsule]]
**Secondary changes such as [[hemorrhage]], [[calcification]] and cystic degeneration are observed
**[[Secondary]] changes such as [[hemorrhage]], [[calcification]] and cystic degeneration are observed


[[image:Thyroid_Diffuse_Hyperplasia.jpg|thumb|250px|center|By Ed Uthman from Houston, TX, USA (Thyroid, Diffuse Hyperplasia) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons]]
[[image:Thyroid_Diffuse_Hyperplasia.jpg|thumb|250px|center|By Ed Uthman from Houston, TX, USA (Thyroid, Diffuse Hyperplasia) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons]]


==Microscopic Pathology==
==Microscopic Pathology==
Microscopic studies that aid in the histopathological analysis:
Microscopic studies that aid in the [[histopathological]] analysis:
*'''[[Fine needle aspiration cytology]] ([[FNAC]])'''
*'''[[Fine needle aspiration cytology]] ([[FNAC]])'''
*'''Open biopsy'''  
*'''Open biopsy'''  

Revision as of 15:19, 13 October 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Overview

When the TRH-TSH thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland. Increased TSH production is trigerred by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process is continuous, it leads to goiter.

Pathophysiology

Pathogenesis:[1][2][3][4][5][6][7][8][9][10][11]

  • The pathophysiological consequences of goitres results from one of the following:
  • The effect of primary disease causing goitre:
    • The effect depends on the underlying disease

Genetics

  • Thyroglobulin (Tg) gene
  • Thyroid-stimulating hormone receptor (TSHR) gene
  • Na+/I- symporter (NIS) gene [18]

Associated Conditions

The following conditions are associated with goiter:

Gross Pathology

By Ed Uthman from Houston, TX, USA (Thyroid, Diffuse Hyperplasia) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

Microscopic Pathology

Microscopic studies that aid in the histopathological analysis:

Histologic Findings:

  • Simple nontoxic goiters demonstrate:
  • Nodular hyperplasia is commonly seen in multinodular goiter. Cytologic findings include:


By Ed Uthman from Houston, TX, USA (Diffuse Thyroid Hyperplasia Uploaded by CFCF) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

References

  1. ↑ Rapoport, Basil (1991). "Pathophysiology of Hashimoto's Thyroiditis and Hypothyroidism". Annual Review of Medicine. 42 (1): 91–96. doi:10.1146/annurev.me.42.020191.000515. ISSN 0066-4219.
  2. ↑ Larsen, P.R. (1972). "Triiodothyronine: Review of recent studies of its physiology and pathophysiology in man". Metabolism. 21 (11): 1073–1092. doi:10.1016/0026-0495(72)90038-8. ISSN 0026-0495.
  3. ↑ Gaitan, Eduardo; Wahner, Heinz W.; Cuello, Carlos; Correa, Pelayo; Jubiz, William; Gaitan, Jorge E. (1969). "Endemic Goiter in the Cauca Valley: II. Studies of Thyroid Pathophysiology1". The Journal of Clinical Endocrinology & Metabolism. 29 (5): 675–683. doi:10.1210/jcem-29-5-675. ISSN 0021-972X.
  4. ↑ Elte JW, Bussemaker JK, Haak A (1990). "The natural history of euthyroid multinodular goitre". Postgrad Med J. 66 (773): 186–90. PMC 2429462. PMID 2114018.
  5. ↑ Berghout A, Wiersinga WM, Smits NJ, Touber JL (1990). "Interrelationships between age, thyroid volume, thyroid nodularity, and thyroid function in patients with sporadic nontoxic goiter". Am. J. Med. 89 (5): 602–8. PMID 2239979.
  6. ↑ Soto, Roberto J.; Imas, Berta; Brunengo, Ana M.; Goldberg, David; Burian, Rosa; Gnocchi, Luisa (1967). "Endemic Goiter in Misiones, Argentina: Pathophysiology Related to Immunological Phenomena". The Journal of Clinical Endocrinology & Metabolism. 27 (11): 1581–1587. doi:10.1210/jcem-27-11-1581. ISSN 0021-972X.
  7. ↑ Gärtner R, Dugrillon A (1998). "[From iodine deficiency to goiter. Pathophysiology of iron deficiency goiter]". Internist (Berl) (in German). 39 (6): 566–73. PMID 9677510.
  8. ↑ Peteiro-Gonzalez, D.; Lee, J.; Rodriguez-Fontan, J.; Castro-Piedras, I.; Cameselle-Teijeiro, J.; Beiras, A.; Bravo, S. B.; Alvarez, C. V.; Hardy, D. M.; Targovnik, H. M.; Arvan, P.; Lado-Abeal, J. (2010). "New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter". The Journal of Clinical Endocrinology & Metabolism. 95 (7): 3522–3526. doi:10.1210/jc.2009-2109. ISSN 0021-972X.
  9. ↑ Capen, C.C. (1992). "Pathophysiology of chemical injury of the thyroid gland". Toxicology Letters. 64-65: 381–388. doi:10.1016/0378-4274(92)90211-2. ISSN 0378-4274.
  10. ↑ Maceri, Dennis R.; Sullivan, Michael J.; McClatchney, Kenneth D. (1986). "AUTOIMMUNE THYROIDITIS". The Laryngoscope. 96 (1): 82???86. doi:10.1288/00005537-198601000-00015. ISSN 0023-852X.
  11. ↑ Neumann, Susanne; Willgerodt, Helmut; Ackermann, Frank; Reske, Andreas; Jung, Martin; Reis, André; Paschke, Ralf (1999). "Linkage of Familial Euthyroid Goiter to the Multinodular Goiter-1 Locus and Exclusion of the Candidate Genes Thyroglobulin, Thyroperoxidase, and Na+/I−Symporter1". The Journal of Clinical Endocrinology & Metabolism. 84 (10): 3750–3756. doi:10.1210/jcem.84.10.6023. ISSN 0021-972X.
  12. ↑ Brix TH, Hegedüs L (2000). "Genetic and environmental factors in the aetiology of simple goitre". Ann. Med. 32 (3): 153–6. PMID 10821321.
  13. ↑ Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N (2003). "The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance". Endocr. Rev. 24 (1): 48–77. doi:10.1210/er.2001-0029. PMID 12588808.
  14. ↑ Targovnik, Héctor M.; Esperante, Sebastián A.; Rivolta, Carina M. (2010). "Genetics and phenomics of hypothyroidism and goiter due to thyroglobulin mutations". Molecular and Cellular Endocrinology. 322 (1–2): 44–55. doi:10.1016/j.mce.2010.01.009. ISSN 0303-7207.
  15. ↑ Spitzweg, Christine; Morris, John C. (2010). "Genetics and phenomics of hypothyroidism and goiter due to NIS mutations". Molecular and Cellular Endocrinology. 322 (1–2): 56–63. doi:10.1016/j.mce.2010.02.007. ISSN 0303-7207.
  16. ↑ Moreno, José C.; Visser, Theo J. (2010). "Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations". Molecular and Cellular Endocrinology. 322 (1–2): 91–98. doi:10.1016/j.mce.2010.03.010. ISSN 0303-7207.
  17. ↑ Fraser GR (1969). "The genetics of thyroid disease". Prog Med Genet. 6: 89–115. PMID 4980080.
  18. ↑ Portulano C, Paroder-Belenitsky M, Carrasco N (2014). "The Na+/I- symporter (NIS): mechanism and medical impact". Endocr Rev. 35 (1): 106–49. doi:10.1210/er.2012-1036. PMC 3895864. PMID 24311738.
  19. ↑ MORTENSEN JD, WOOLNER LB, BENNETT WA (1955). "Gross and microscopic findings in clinically normal thyroid glands". J Clin Endocrinol Metab. 15 (10): 1270–80. doi:10.1210/jcem-15-10-1270. PMID 13263417.
  20. ↑ "Reorganized text". JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
  21. ↑ Hegedüs L, Bonnema SJ, Bennedbaek FN (2003). "Management of simple nodular goiter: current status and future perspectives". Endocr Rev. 24 (1): 102–32. doi:10.1210/er.2002-0016. PMID 12588812.

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